Introduction: In insulin resistance animal models, insulin uptake from periphery to the brain is impaired. While insulin is not involved in glucose transfer to the neurons, it is required for neuron survival and function through binding to its receptor. Furthermore, an insulin homologue called insulin like growth factor (IGF-I) is abundantly expressed in mature rats, acts in parallel with the insulin in brain, binds to the insulin receptor and its serum levels reduced in insulin resistance. In this study, we sought to investigate whether the expression of brain IGF-I is altered in the insulin resistant animal model. Materials and Methods Wistar rats were fed with 10% fructose in their drinking water up to 4 months and induced with the insulin resistance. The rats were killed, perfused with 4% PFA, and their brains were sectioned and studied for the immunoreactivity of the IGF-I. Results: Results showed that there is an increased intensity of IGF-I in most brain areas. Conclusion: Altogether, despite the low levels or lack of insulin in brain of the insulin resistant animal model, increased expression of the brain suggests a compensatory mechanism to maintain the insulin function.